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PubMed1999

Effect of substance P on histamine secretion from gut mucosa in inflammatory bowel disease.

BACKGROUND: Mast cell hyperplasia in the gut is a feature of inflammatory bowel disease (IBD), but the role of mast cells in this disease is still unclear. Since mast cell-nerve interactions might have some impact on intestinal inflammation, the present study investigated whether the neuropeptide substance P causes histamine secretion from human gut mucosal mast cells. METHODS: Four hundred and eighteen colorectal endoscopic samples from 20 patients with IBD and 10 controls were studied. Colorectal biopsy samples were cultured in an oxygenated medium for spontaneous histamine release or were stimulated with substance P, anti-human immunoglobulin E, and a combination of substance P and anti-human immunoglobulin E. Histamine release was measured using a highly sensitive and specific radioimmunoassay. RESULTS: Substance P failed to induce mast cell activation in histologically normal mucosa from controls. In contrast, mucosal specimens taken from inflamed IBD tissue or from uninvolved Crohn disease tissue showed a considerably enhanced rate of histamine secretion towards substance P, alone or in combination with anti-IgE. Unaffected mucosa with ulcerative colitis appeared insensitive towards substance P. CONCLUSIONS: The neuropeptide substance P was shown to preferentially enhance mucosal mast cell mediator secretion in active IBD. Thus, it appears likely that mast cell-nerve interactions are involved in as yet uninvestigated neurovegetative histamine-releasing processes of the gut in IBD.

Adult↗

PubMed1999

Evaluation of serological, histological and immunocytochemical methods for the detection of infectious bursal disease virus infection in broiler flocks in New Zealand.

AIMS: TO study and compare three diagnostic methods for the detection of infectious bursal disease virus (IBDV) infection. METHODS: Samples of sera and bursae were collected from two flocks from each of two broiler farms (Farms A and B) in which IBD had occurred or was suspected to have occurred. Sera were tested in ELISA and agar gel precipitation tests for the presence of IBD antibodies. Bursae were examined histologically for evidence of IBD lesions. An immunocytochemical test was developed to detect IBDV antigens in sections of bursa. RESULTS: Bursae from serologically negative, 45-day-old birds from Farm A, Flock 1 and from serologically positive 49-day-old birds from Farm B, Flock 1 had histological and immunocytochemical evidence of IBDV infection. Birds from Farm A, Flock 2, sampled 12 months after the sampling of Flock 1, and specific-pathogen-free birds, showed no evidence of IBDV infection by any of the three diagnostic methods. Birds from Farm B, Flock 2, sampled on four occasions, were positive for IBD at 20 days of age by histology and immunocytochemistry, but did not seroconvert until 42 days of age. CONCLUSIONS: Serological testing is not a reliable method for the detection of IBDV infection in New Zealand broiler flocks because antibodies may not have developed to detectable levels by the time of slaughter. Histological examination of bursae allowed the demonstration of IBD-like lesions, but these need to be differentiated from those caused by other agents. The immunocytochemistry test was able to detect early IBDV infection. It provided a rapid, definitive diagnosis and may be useful in control programmes. The results from Farm A demonstrate that strict biosecurity measures can be successful in the eradication of IBDV.

Journal Article↗

PubMed2002

Risk factors associated with the introduction of acute clinical infectious bursal disease among Danish broiler chickens in 1998.

The objective of the present study was to investigate risk factors associated with the introduction of acute clinical infectious bursal disease (IBD) among Danish broiler chickens in 1998. Data on 218 flocks were collected from hatcheries, abattoirs, farmers and veterinarians; 49 of the flocks had experienced acute clinical IBD (cases), 169 were unexposed (controls). The study was carried out using a case-control design. Cases were defined as the first flock on each premises to experience acute clinical IBD, and these were compared with non-diseased, non-IBD-vaccinated control flocks chosen randomly from each unaffected farm. The resulting numbers of cases and controls used for statistical analyses were 16 and 61, respectively. Statistically significant associations were seen between the initial 16 Danish cases of acute clinical IBD in 1998 and certain hatcheries, age of parent birds and a certain feed mill.

Abattoirs↗

PubMed2002

Antigranulocyte monoclonal antibody immunoscintigraphy in inflammatory bowel disease in children and young adolescents.

AIM: Diagnostic delay for inflammatory bowel disease (IBD) is frequent, especially in paediatric patients. Scintigraphy with labelled leucocytes has been proposed as a very sensitive diagnostic tool for detecting bowel inflammation. The aim of this study was to evaluate the sensitivity and specificity of immunoscintigraphy in the diagnosis and follow-up of children with IBD and to compare this technique with other diagnostic techniques. METHODS: Sixty-six children with histologically confirmed IBD were enrolled in the study. Twenty-one children in whom IBD was suspected but subsequently not confirmed were used as controls. A total of 138 immunoscintigraphies were performed using 99mTechnetium-labelled monoclonal anti-granulocyte antibodies. Immunoscintigraphy was also compared with other diagnostic techniques. RESULTS: Overall sensitivity of monoclonal antibody immunoscintigraphy (MoAb-IS) in patients with clinically active disease was 94% for Crohn's disease (CD) and 85% for ulcerative colitis (UC). Ultrasonography, endoscopy and radiology were carried out at the same time in 29 patients with CD and in 6 patients with UC: sensitivity of IS was 90% compared with 76% of colonoscopy, 75% for enemas, and 55% for sonography. IS was negative (specificity) in 24% of patients with CD and in 67% of patients with UC during remission, and in 64% of controls with other causes of intestinal inflammation. Diagnostic delay was significantly shorter when compared with a historical cohort of patients. CONCLUSION: Immunoscintigraphy is a highly sensitive detector of intestinal inflammation in young patients with IBD and can be useful for reducing diagnostic delay. However, its specificity is low and all positive cases must be confirmed histologically.

Adolescent↗

PubMed2003

Crohn's-like ileo-colitis in patients affected by glycogen storage disease Ib: two years' follow-up of patients with a wide spectrum of gastrointestinal signs.

AIM: To investigate the presence of inflammatory bowel disease (IBD) and to evaluate the progression of bowel involvement after two years' follow-up in seven patients affected by glycogen storage disease type Ib (GSDIb). METHODS: Seven patients (5F, 2M, aged 4.5-20.6 y) entered the study. Bowel involvement was evaluated by ileocolonoscopy and specific IBD serologic markers. To evaluate disease activity, Paediatric Crohn's Disease Activity Index (PCDAI), terminal ileum wall thickness detected at ultrasonography (US), 99mTechnetium labelled autologous White Cell Scan (Tc-WCS) and barium meal with follow-through were investigated. RESULTS: Ileocolonoscopy and histology examination revealed variable degrees of bowel involvement in all patients. The results of serologic markers were indicative of a Crohn's-like ileocolitis. US and Tc-WCS, could clearly define patients with severe inflammatory involvement, but failed to identify all patients with mild to moderate disease. For the most severely affected patients, anti-inflammatory agents and steroids were prescribed, whereas nutritional therapy with polymeric formula and antibiotics were assumed by two other patients and antibiotics only by one patient. Granulocyte colony-stimulating factor (G-CSF) was prescribed to all patients. Ileocolonoscopy and histology data improved in all patients. The assumption of G-CSF and/or gastric drip feeding (g.d.f.) was inversely associated with the PCDAI results (p < 0.05). CONCLUSION: IBD is common in patients affected by GSDIb independently of the severity of gastrointestinal signs and symptoms. Different therapeutic approaches can be used according to the severity of IBD. G-CSF treatment and g.d.f. can be protective factors for IBD.

Adolescent↗

PubMed2001

Recent advances in inflammatory bowel disease.

The last decade has seen tremendous advances in our knowledge, which has led to genuine improvements in our understanding of the pathogenesis and management of inflammatory bowel disease (IBD). The combined power of cellular and molecular biology has begun to unveil the enigmas of IBD, and, consequently, substantial gains have been made in the treatment of IBD. Refinements in drug formulation have provided the ability to target distinct sites of delivery, while enhancing the safety and efficacy of older agents. Simultaneous progress in biotechnology has fostered the development of new agents that strategically target pivotal processes in disease pathogenesis. This article addresses our current understanding of the pathogenesis of IBD, including the latest developments in animal models and covers agents currently used in the treatment of IBD as well as emerging therapies.

Animals↗

PubMed1996

Role of appendix in the development of inflammatory bowel disease in TCR-alpha mutant mice.

T cell receptor-alpha mutant mice (TCR-alpha-/-), created by gene targeting of the TCR-alpha gene in embryonic stem cells, spontaneously develop inflammatory bowel disease (IBD) resembling human ulcerative colitis. Since gut-associated lymphoid tissue is likely to play an important role in the development of chronic intestinal inflammation, we examined the changes in the appendix lymphoid follicle (ALF) and Peyer's patches (PP) in these mice. We found the structure of the ALF to be remarkably similar to that of the PP in the small intestine; in both instances, lymphoid follicles covered by surface epithelium (dome-formation) were found. The amount of proliferation in the lymphoid follicles of the appendix estimated by in vivo incorporation of 5-bromo-2'deoxyuridine was more than two times that of PP in TCR-alpha-/- mice. ELISPOT assay showed an increase of IgA, IgG1, and IgG2a, but not IgM-secreting B cells in ALF of TCR-alpha-/- mice compared to TCR-alpha+/- control mice. Furthermore, TCR-alpha-/- mice revealed an increase of autoantibody-producing B cells against the cytoskeletal protein tropomyosin in ALF as compared to PP. When TCR-alpha-/- mice underwent appendectomy at a young age (3-5 wk), the number of mesenteric lymph nodes cells at 6-7 mo were markedly less than in the sham-operated TCR-alpha-/- mice. Furthermore, appendectomy at 1 mo of age suppressed the development of IBD, with only 3.3% of these mice developing IBD in the 6-7-mo period of observation. In contrast, approximately 80% of controls, including the sham-operated TCR-alpha-/- mice, developed IBD during this period. These results suggest that ALF, rather than PP, is the priming site of cells involved in the disease process and plays an important role in the development of IBD in TCR-alpha-/- mice.

Animals↗

PubMed2003

MDR1 Ala893 polymorphism is associated with inflammatory bowel disease.

Crohn disease (CD) and ulcerative colitis (UC) are overlapping chronic inflammatory bowel diseases (IBDs). Suggestive evidence for linkage at chromosome 7q has been reported for both CD and UC. Contained within this region is the gene for MDR1 (multidrug resistance), a membrane transport protein for which human polymorphisms have been reported in Ala893Ser/Thr and C3435T that alter pharmacokinetic profiles for a variety of drugs. Because mdr1 knockout mice spontaneously develop colitis, exonic regions were resequenced and tested for IBD association in a large, multicenter North American cohort. Two missense mutations, Asn21Asp and Ala893Ser/Thr, as well as the expression-associated polymorphism C3435T, described elsewhere, were genotyped in the entire cohort. Significant association of Ala893 with IBD was observed by both case-control analysis (P=.002) and the pedigree disequilibrium test (PDT [P=.00020-.00030]) but not for the Asn21Asp or C3435T polymorphisms. Significant association by PDT was observed within the subset with CD (P=.0014-.00090), with similar, nonsignificant trends in a smaller subset with UC. The Ala893Ser/Thr variant is triallelic, and the associated, common allele is Ala893, with undertransmission of the 893Ser (common) and the 893Thr (rare) variants. The Ala893 variant has decreased activity compared with the 893Ser variant; therefore, the association with human IBD is consistent with the murine model of mdr1 deficiency. Taken together, these data support the association of the common Ala893 polymorphism with IBD specifically and, more broadly, provides additional support for its contribution to interindividual pharmacogenetic variation.

Alanine↗

PubMed2001

On relationship inference using gamete identity by descent data.

Related individuals are identical by descent (IBD) at a genetic locus if they share the same DNA material from a common ancestor. Continuous gamete IBD data consist of the lengths of (in order) IBD and non-IBD regions along the genomes for gametes segregating from two related individuals and can be used to distinguish different relationships. Under the assumption that the crossovers follow a Poisson process, we show that the exact calculation of the likelihood of a particular relationship for a given gamete IBD datum is tractable. Greatgrandparent--greatgrandchild and cousin relationships are used as examples to illustrate our methods.

Computer Simulation↗

PubMed1997

Dairy sensitivity, lactose malabsorption, and elimination diets in inflammatory bowel disease.

The ability of inflammatory bowel disease (IBD) patients to tolerate dairy products and the guidance they receive from physicians and nutritionists on this subject are important considerations in the management of their IBD. Although most affected persons are able to consume a glass of milk daily without discomfort, additional consideration must be given to specific factors that can be relevant to certain individuals. The declaration by patients that they are "dairy sensitive" may be related to lactose intolerance or malabsorption, the long-chain triacylglycerol content of milk, allergy to milk proteins, as well as psychologic factors and the misconception that dairy products can be detrimental to their health. The prevalence of lactose malabsorption is significantly greater in patients with Crohn disease involving the small bowel than it is in patients with Crohn disease involving the colon or ulcerative colitis. In the latter colonic conditions the prevalence of lactose malabsorption is mainly determined by ethnic risk, which is based on genetic factors. In addition, lactose malabsorption in Crohn disease of the small bowel may be determined by factors other than lactase enzyme activity, such as bacterial overgrowth and/or small bowel transit time. Physicians differ widely in the advice they give their patients: some dogmatically advise avoidance of dairy products when the diagnosis is made whereas others discount the possible role of dairy in the management of IBD. IBD patients avoid dairy products more than they would need to based on the prevalence of lactose malabsorption and/or milk intolerance, probably partly because of incorrect patient perceptions and arbitrary advice from physicians and authors of popular diet books. Adequate scientific and clinical information is now available to permit recommendations about the intake of dairy products for each IBD patient.

Humans↗

PubMed2002

Inflammatory bowel disease is associated with a TNF polymorphism that affects an interaction between the OCT1 and NF(-kappa)B transcription factors.

Tumour necrosis factor-alpha (TNF) expression is increased in inflammatory bowel disease (IBD), and TNF maps to the IBD3 susceptibility locus. Transmission disequilibrium and case-control analyses, in two independent Caucasian cohorts, showed a novel association of the TNF(-857C) promoter polymorphism with IBD (overall P=0.001 in 587 IBD families). Further genetic associations of TNF(-857C) with IBD sub-phenotypes were seen for ulcerative colitis and for Crohn's disease, but only in patients not carrying common NOD2 mutations. The genetic data suggest a recessive model of inheritance, and we observed ex vivo lipopolysaccharide-stimulated whole-blood TNF production to be higher in healthy TNF(-857C) homozygotes. We show the transcription factor OCT1 binds TNF(-857T) but not TNF(-857C), and interacts in vitro and in vivo with the pro-inflammatory NF(-kappa)B transcription factor p65 subunit at an adjacent binding site. Detailed functional analyses of these interactions in gut macrophages, in addition to further genetic mapping of this gene-dense region, will be critical to understand the significance of the observed association of TNF(-857C) with IBD.

Animals↗

PubMed2003

Functional annotation of a novel NFKB1 promoter polymorphism that increases risk for ulcerative colitis.

Nuclear Factor-kappaB (NF-kappaB) is a major transcription regulator of immune response, apoptosis and cell-growth control genes, and is upregulated in inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease. The NFKB1 gene encodes the NF-kappaB p105/p50 isoforms. Genome-wide screens in IBD families show evidence for linkage on chromosome 4q where NFKB1 maps. We sequenced the NFKB1 promoter, exon 1 and all coding exons in 10 IBD probands and two controls, and identified six nucleotide variants, including a common insertion/deletion promoter polymorphism (-94ins/delATTG). Using pedigree-based transmission disequilibrium tests, we observed modest evidence for linkage disequilibrium (LD), independent of linkage, between the -94delATTG allele and UC in 131 out of 235 IBD pedigrees with UC offspring (P=0.047-0.052). This allele was also more frequent in the 156 non-Jewish UC probands from the 235 IBD pedigrees than in 149 non-Jewish controls (P=0.015). The -94delATTG association with UC was replicated in a second set of 258 unrelated, non-Jewish UC cases and 653 new, non-Jewish controls (P=0.021). Nuclear proteins from normal human colon tissue and colonic cell lines, but not ileal tissue, showed significant binding to -94insATTG but not to -94delATTG containing oligonucleotides. NFKB1 promoter/exon 1 luciferase reporter plasmid constructs containing the -94delATTG allele and transfected into either HeLa or HT-29 cell lines showed less promoter activity than comparable constructs containing the -94insATTG allele. Therefore, we have identified the first potentially functional polymorphism of NFKB1 and demonstrated its genetic association with a common human disease, ulcerative colitis.

Base Sequence↗

PubMed2025

Disparities in Outcomes for Patients With Inflammatory Bowel Disease at a Private vs Public Hospital in New York City.

BACKGROUND: In patients with inflammatory bowel disease (IBD), social determinants of health contribute to health inequalities. We aimed to compare patients with IBD treated at a private nonprofit vs public hospital in New York City. METHODS: We performed a retrospective study of adult patients with Crohn's disease or ulcerative colitis with established IBD care. Patient demographics, disease characteristics, healthcare utilization, treatment modalities, and clinical outcomes were collected. Using a series of linear mixed and logistic models, the differences between care at a private nonprofit vs public hospital were assessed while controlling for factors that differed between them. RESULTS: Our study included 418 patients with IBD, 209 from each hospital. Compared with public hospital patients, private hospital patients were more likely to be White, be non-Hispanic, and have private insurance (all P = .0005) and less likely to face housing instability (P < .0001), face unemployment (P = .0004), be current smokers (P = .03), or be foreign born (P < .0001). Patients at the private hospital were more likely to have multiple anti-tumor necrosis factor (P = .0001) and biologic use (P < .0001). Public hospital patients were less likely to be considered endoscopically adherent (odds ratio [OR], 0.377; P = .001) and more likely to visit the emergency department (OR, 5.01; P < .0001) and be hospitalized (OR, 1.92; P = .05). CONCLUSIONS: Our study is the first to identify significant differences in patient demographics, disease phenotype, treatments and clinical outcomes between patients treated for IBD at a private nonprofit vs public hospital. Our data suggest that social determinants of health drive disparities in the utilization of healthcare facilities.

Humans↗

PubMed1996

Incidence of inflammatory bowel disease in Italy: a nationwide population-based study. Gruppo Italiano per lo Studio del Colon e del Retto (GISC)

BACKGROUND: The epidemiology of inflammatory bowel disease (IBD) in Southern Europe is still unclear. Sporadic reports suggest a lower incidence of IBD in Italy than in other Western Countries and the USA. METHODS: A nationwide population-based study was carried out to estimate IBD incidence rates in eight Italian cities. All new cases of IBD diagnosed over 4 years in the target populations were collected from multiple information sources. RESULTS: From 1989 to 1992, 509 ulcerative colitis (UC), 222 Crohn's disease (CD) and 10 undefined IBD cases were collected, giving age-adjusted incidence rates (per 100,000 per year) of 5.2 for UC and 2.3 for CD. Using the capture-recapture method, an estimated completeness of 0.81 was obtained for case archives, without appreciable and significant differences between areas. The rates computed after correcting underestimation were 6.8 for UC and 2.8 for CD. The sex ratio M/F was 1.7 for UC and 1.0 for CD. The highest age-specific incidence rates were between 30 and 39 years for UC and between 20 and 29 years for CD. CONCLUSIONS: The incidence rate of CD in italy is homogeneous between the cities investigated and lower than those reported for other Mediterranean countries. In contrast, the UC incidence rate is within the range of those reported in European studies. A wide variability in the UC rates between the cities was also observed. These results could be related to different environmental factors or the genetic background of the populations, or both.

Adolescent↗

PubMed2000

1,25-Dihydroxycholecalciferol prevents and ameliorates symptoms of experimental murine inflammatory bowel disease.

Anecdotal data suggest that the amount of vitamin D available in the environment either from sunshine exposure or diet may be an important factor affecting the development of inflammatory bowel disease (IBD) in humans. We tested the vitamin D hypothesis in an experimental animal model of IBD. Interleukin (IL)-10 knockout (KO) mice, which spontaneously develop symptoms resembling human IBD, were made vitamin D deficient, vitamin D sufficient or supplemented with active vitamin D (1,25-dihydroxycholecalciferol). Vitamin D-deficient IL-10 KO mice rapidly developed diarrhea and a wasting disease, which induced mortality. In contrast, vitamin D-sufficient IL-10 KO mice did not develop diarrhea, waste or die. Supplementation with 50 IU of cholecalciferol (5.0 microgram/d) or 1, 25-dihydroxycholecalciferol (0.005 microgram/d) significantly (P < 0. 05) ameliorated symptoms of IBD in IL-10 KO mice. 1, 25-Dihydroxycholecalciferol treatment (0.2 microgram/d) for as little as 2 wk blocked the progression and ameliorated (P < 0.05) symptoms in IL-10 KO mice with already established IBD.

Analysis of Variance↗

PubMed2004

Review: psychosocial issues in pediatric inflammatory bowel disease.

OBJECTIVE: To review and critically evaluate research on psychosocial issues in pediatric inflammatory bowel disease (IBD) and to provide recommendations for future research. METHODS: A literature search was conducted using the Medline and PsychInfo computerized databases as well as the bibliographies of relevant articles. RESULTS: Most of the existing research has compared children with IBD to healthy populations and other illness populations. Compared to healthy children, children with IBD may be at greater risk for difficulties in behavioral and emotional functioning as well as in family and parent functioning, but all such functioning appears similar to that found in other illness populations. It is unclear if the increased risk reaches clinical significance and what role the severity of the disease plays in adjustment. CONCLUSIONS: Future research should use a developmental perspective to investigate the process of adaptation to IBD, risk factors of poor adjustment, and the role of psychosocial factors in health outcomes in pediatric IBD.

Adaptation, Psychological↗

PubMed2005

Brief report: psychosocial adjustment in adolescents with inflammatory bowel disease.

BACKGROUND: Inflammatory bowel disease (IBD) is an ideal disease for investigating adolescent adjustment to chronic illness, given its embarrassing, socially limiting, appearance-changing symptoms and adolescent onset. OBJECTIVE: To compare psychosocial adjustment among adolescents with a chronic illness to that of healthy adolescents and examine the role of adolescent disease onset. METHODS: Participants were 50 adolescents with IBD and their parents, and parents of 42 healthy comparison adolescents who completed questionnaires assessing behavioral, emotional, social, and family functioning. RESULTS: Adolescents with IBD were reported to have worse anxious and/or depressed and social problems than healthy adolescents. More adolescents with IBD were reported to have clinically significant social problems. Those diagnosed during adolescence were reported to have significantly worse social competence scores. CONCLUSIONS: Adolescents with a chronic illness such as IBD may be at higher risk for specific psychosocial difficulties than healthy adolescents. Diagnosis of a chronic illness during adolescence may have implications for social functioning.

Adaptation, Psychological↗

PubMed2000

Altered IgG(4) renal clearance in patients with inflammatory bowel diseases. Evidence for a subclinical impairment of protein charge renal selectivity.

BACKGROUND: A loss of intestinal glycosaminoglycans (GAGs) has been shown in inflammatory bowel diseases (IBD). Since GAGs are involved in the regulation of renal protein filtration and GAGs disruption is associated with anionic proteinuria, we examined whether changes in the selectivity of renal protein filtration occur in IBD. METHODS: From 46 patients with IBD (17 with Crohn's disease (CD), and 29 with ulcerative colitis (UC)) and 21 healthy subjects, urine and serum samples were obtained. Albumin, total IgG and IgG(4) clearances were measured using sensitive methods. Serum p-ANCA and TNF-alpha were tested. RESULTS: Median IgG(4) clearance was 0.041 ml/ min/10(-3) in patients with UC and 0.10 ml/ min/10(-3) in CD patients, both significantly higher than in controls (0.03 ml/min/10(-3)) (P<0.03). IgG(4) clearance was above the upper normal limit in 9/17 CD (53%) and in 10/29 UC (34.5%). Eighteen of 19 patients showing abnormal IgG(4) clearance were taking mesalazine. In patients on maintenance oral mesalazine, IgG(4) clearance was higher than that in patients off treatment (0.12 vs 0.03 ml/min/10(-3), P=0.04). No clinical/laboratory sign of renal dysfunction was documented in patients with altered IgG(4) clearance and maintained on mesalazine treatment. CONCLUSION: Renal protein charge permselectivity is impaired in 40% of patients with IBD with no overt proteinuria. Our data suggest that altered IgG(4) clearance may represent a subclinical marker of renal involvement in IBD.

Administration, Oral↗